Stroke is the third most common cause of death in the United States and the most disabling neurologic disorder. Approximately 700,000 patients suffer from stroke annually. Stroke is a syndrome characterized by the acute onset of a neurological deficit that persists for at least 24 hours, reflecting focal involvement of the central nervous system, and is the result of a disturbance of the cerebral circulation. Its incidence increases with age. Risk factors for stroke include systolic or diastolic hypertension, hypercholesterolemia, cigarette smoking, heavy alcohol consumption, and oral contraceptive use.
Eighty percent strokes are ischemic strokes and are caused by occluded vessels that deprive the brain of oxygen-carrying blood (the remaining 20% of strokes are hemorrhagic strokes, which result in bleeding into the brain). Ischemic strokes are often caused by emboli or pieces of thrombotic tissue that have dislodged from other body sites or from the cerebral vessels themselves to occlude in the narrow cerebral arteries more distally. When a patient presents with neurological symptoms and signs, which resolve completely within 1 hour, the term transient ischemic attack (TIA) is used. Etiologically, TIA and ischemic stroke share the same pathophysiologic mechanisms and thus represent a continuum based on persistence of symptoms and extent of ischemic insult.
Emboli occasionally form around the valves of the heart or in the left atrial appendage during periods of irregular heart rhythm and then are dislodged and follow the blood flow into the distal regions of the body. Those emboli can pass to the brain and cause an embolic stroke. Many such occlusions occur in the middle cerebral artery (MCA), although such is not the only site where emboli come to rest.
Ischemic stroke is sometimes treated by injecting tissue plasminogen activator (t-PA) or Activase® into the patient's blood stream. However, treatment with systemic t-PA is associated with increased risk of intracerebral hemorrhage and other hemorrhagic complications. Patients treated with t-PA are more likely to sustain a symptomatic intracerebral hemorrhage during the first 36 hours of treatment. The frequency of symptomatic hemorrhage increases when t-PA is administered beyond 3 hours from the onset of a stroke. Besides the time constraint in using t-PA in acute ischemic stroke, other contraindications include the following: if the patient has had a previous stroke or serious head trauma in the preceding 3 months, if the patient has a systolic blood pressure above 185 mmHg or diastolic blood pressure above 110 mmHg, if the patient requires aggressive treatment to reduce the blood pressure to the specified limits, if the patient is taking anticoagulants or has a propensity to hemorrhage, and/or if the patient has had a recent invasive surgical procedure. Therefore, only a small percentage of selected stroke patients are qualified to receive t-PA.
Stroke is sometimes treated by attempting to re-establish blood flow in the blocked artery. Certain percutaneous methods have been utilized for reestablishing blood flow. A common percutaneous technique is referred to as balloon angioplasty where a balloon-tipped catheter is introduced to a blood vessel, advanced to the point of the occlusion and inflated in order to dilate the stenosis. Balloon angioplasty is appropriate for treating vessel stenosis but is not effective for treating acute thromboemboli. In patients with vertebral artery occlusions, treatment with angioplasty often results in disastrous complications due to embolization of the occlusive lesion downstream to the basilar artery. Emboli small enough to pass through the vertebral arteries into the larger basilar artery are usually arrested at the top of the basilar artery, where it bifurcates into the posterior cerebral arteries. The resulting reduction in blood flow to the ascending reticular formation of the midbrain and thalamus produces immediate loss of consciousness.
Another percutaneous technique is to place a microcatheter near the clot and infuse streptokinase, urokinase or other thrombolytic agents to dissolve the clot. Unfortunately, thrombolysis typically takes hours to days to be successful. Additionally, thrombolytic agents can cause severe hemorrhage and in many patients the agents cannot be used at all.
Another percutaneous technique is to place a guide catheter proximate the clot and aspirate the clot into the guide catheter. This procedure requires that the guide catheter be brought into close proximity of the clot in order to be effective. Proper placement may be difficult or impossible. Furthermore, a highly aggregated, cohesive clot may not easily be aspirated into a guide catheter without prior thrombolysis or breakdown into small pieces.
Yet another percutaneous technique is to place an expandable structure, located at or near the distal end of a catheter, through a vessel obstruction and expand that structure. The expandable structure can be used to pull the clot back into a guide catheter with its open end placed nearby. Activation of the expandable structure, however, using linkages or other mechanisms can be difficult to perform or control due to the high amount of friction present in a long cerebrovascular catheter with extremely small lumens.
Another problematic area is the removal of foreign bodies. Foreign bodies introduced into the circulation can be fragments of catheters, pacemaker electrodes, guide wires, and erroneously placed embolic material such as thrombogenic coils. The use of such removal devices is difficult and sometimes unsuccessful.
Thus, there exists a need for the development of a device that can be percutaneously introduced, endovascularly advanced to the target lesion, moved across or into the obstruction, and deployed in a controlled, reliable manner into the circulatory system for the removal of viscoelastic clots and foreign bodies without the risk of clot disgorgement, flaking, or incomplete removal. The system needs to, then, be retracted, along with the obstruction from the target vessel. There is also a need for a device, which could be used as a temporary arterial or venous filter to capture and remove thromboemboli formed during endovascular procedures.